1. Motor Unit EMG
Motor Unit EMG
Von Willebrand Disease
Josh Rice, Allison August, Nori McKinney, Aundrea Berdahl
Lab section 1 , Life 102 Lab, Stacy Endriss, Colorado State University
Genetic Basis
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*Is is Treatable?
Symptoms
Is the Disorder Common?
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•Sensitive bruising
•Reoccurring nosebleeds
•Extensive bleeding especially after severe cuts or
surgery
•Bleeding that secretes into joints, intestines, or
stomach
The severity of the disease was classified as Type I,
Type II, and Type III. Its symptoms were decided in
ascending order by what was physically obvious is
the disorder. All the symptoms were not guaranteed
via type. Depending on the patent, if diagnosed with
Type III, they could have any or all of the signs.
From ancestor to ancestor in the punnet square of
life, each generation’s severity can be moderate or
mild to heavy flow (Z.M. Ruggeri, 1998).
(Ginsburg, 1991)
Unfortunately, there is no cure. Once a person
is diagnosed with Von Willebrand’s Disease
they will have it for their entire lives. (Ginsburg, 1991)
Von Willebrand disease is a hereditary bleeding
disorder in which the von Willebrand factor is deficient.
The von Willebrand factor helps blood platelets clot,
clump together, and stick to the vessel wall. Von
Willebrand disease can be received from either parent.
The offspring of an individual with von Willebrand
disease is about fifty percent. The diagnosis test
entails bleeding time, blood time, platelet count,
and Von Willebrand-specific tests of an individual.
(National Hemoplilia Foundation, 2006). The disease is
present in approximately one to two percent of the
population. A Finnish physician, Erik von Willebrand,
first defined the disease. Von Willebrand disease is
most popularly categorized into four forms: Type I is
the least severe and most common type of von
Willebrand disease. Type II is unique because is has
an abnormality in itself. The abnormality of von
Willebrand creates Type IIa and Type IIb subtypes.
What creates the abnormality is factor VIII, which is
essentially a coagulant protein. In Type IIa, the factor is
reduced, whereas Type IIb has an absence of factor
VIII. Type III is the most hazardous form of von
Willebrand, as only 10% of the normal factor VIII
functioning and there is no von Willebrand factor in the
individual (Gersten, 2012). This disorder resembles
Type IIb von Willebrand disease, but the defects
appear to be in the platelets, rather than the von
Willebrand factor